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International Journal of Chronic... 2022Chronic obstructive pulmonary disease (COPD) includes chronic bronchitis, emphysema, and small airway obstruction. Incompletely reversible airflow limitation,... (Review)
Review
Chronic obstructive pulmonary disease (COPD) includes chronic bronchitis, emphysema, and small airway obstruction. Incompletely reversible airflow limitation, inflammation, excessive mucus secretion and bronchial mucosal epithelial lesions are the main pathological basis of the disease. The prevalence of COPD is increasingly worldwide, which has caused the burden on individuals and society. This paper summarizes the pathogenesis of COPD and clarifies the effect and mechanism of the latest targeted drugs for COPD. Besides, we focus on NOD-like receptor thermal protein domain associated protein 3 inflammasome (NLRP3 inflammasome). NLRP3 can promote production of interleukin-1β (IL-1β) and interleukin-18 (IL-18). NLRP3 is an important factor in the migratory aggregation of macrophages and neutrophils and the generation of oxidative stress. Inhibition of NLRP3 inflammasome indirectly blocks the inflammatory effects of IL-1β and IL-18, which may be regarded as an ideal target for COPD treatment.
Topics: Humans; Inflammasomes; Inflammation; Interleukin-18; Interleukin-1beta; NLR Family, Pyrin Domain-Containing 3 Protein; Pulmonary Disease, Chronic Obstructive
PubMed: 35855746
DOI: 10.2147/COPD.S366126 -
Chinese Medical Journal May 2022Severe asthma is "asthma which requires treatment with high dose inhaled corticosteroids (ICS) plus a second controller (and/or systemic corticosteroids) to prevent it... (Review)
Review
Severe asthma is "asthma which requires treatment with high dose inhaled corticosteroids (ICS) plus a second controller (and/or systemic corticosteroids) to prevent it from becoming 'uncontrolled' or which remains 'uncontrolled' despite this therapy." The state of control was defined by symptoms, exacerbations and the degree of airflow obstruction. Therefore, for the diagnosis of severe asthma, it is important to have evidence for a diagnosis of asthma with an assessment of its severity, followed by a review of comorbidities, risk factors, triggers and an assessment of whether treatment is commensurate with severity, whether the prescribed treatments have been adhered to and whether inhaled therapy has been properly administered. Phenotyping of severe asthma has been introduced with the definition of a severe eosinophilic asthma phenotype characterized by recurrent exacerbations despite being on high dose ICS and sometimes oral corticosteroids, with a high blood eosinophil count and a raised level of nitric oxide in exhaled breath. This phenotype has been associated with a Type-2 (T2) inflammatory profile with expression of interleukin (IL)-4, IL-5, and IL-13. Molecular phenotyping has also revealed non-T2 inflammatory phenotypes such as Type-1 or Type-17 driven phenotypes. Antibody treatments targeted at the T2 targets such as anti-IL5, anti-IL5Rα, and anti-IL4Rα antibodies are now available for treating severe eosinophilic asthma, in addition to anti-immunoglobulin E antibody for severe allergic asthma. No targeted treatments are currently available for non-T2 inflammatory phenotypes. Long-term azithromycin and bronchial thermoplasty may be considered. The future lies with molecular phenotyping of the airway inflammatory process to refine asthma endotypes for precision medicine.
Topics: Adrenal Cortex Hormones; Anti-Asthmatic Agents; Asthma; Eosinophilia; Humans; Patient Acuity; Phenotype
PubMed: 35633594
DOI: 10.1097/CM9.0000000000001990 -
International Journal of Chronic... 2023Chronic respiratory diseases (CRD), is a group of disorders, primarily chronic obstructive pulmonary disease and asthma, which are characterized by high prevalence and... (Review)
Review
Chronic respiratory diseases (CRD), is a group of disorders, primarily chronic obstructive pulmonary disease and asthma, which are characterized by high prevalence and disability, recurrent acute exacerbations, and multiple comorbidities, resulting in exercise limitations and reduced health-related quality of life. Exercise training, an important tool in pulmonary rehabilitation, reduces adverse symptoms in patients by relieving respiratory limitations, increasing gas exchange, increasing central and peripheral hemodynamic forces, and enhancing skeletal muscle function. Aerobic, resistance, and high-intensity intermittent exercises, and other emerging forms such as aquatic exercise and Tai Chi effectively improve exercise capacity, physical fitness, and pulmonary function in patients with CRD. The underlying mechanisms include enhancement of the body's immune response, better control of the inflammatory response, and acceleration of the interaction between the vagus and sympathetic nerves to improve gas exchange. Here, we reviewed the new evidence of benefits and mechanisms of exercise intervention in the pulmonary rehabilitation of patients with chronic obstructive pulmonary disease, bronchial asthma, bronchiectasis, interstitial lung disease, and lung cancer.
Topics: Humans; Pulmonary Disease, Chronic Obstructive; Quality of Life; Lung; Exercise Therapy; Asthma; Respiration Disorders; Exercise Tolerance
PubMed: 37362621
DOI: 10.2147/COPD.S408325 -
American Family Physician Feb 2022Hemoptysis is the expectoration of blood from the lower respiratory tract, usually from bronchial arteries. The most common causes are acute respiratory infections,...
Hemoptysis is the expectoration of blood from the lower respiratory tract, usually from bronchial arteries. The most common causes are acute respiratory infections, cancer, bronchiectasis, and chronic obstructive pulmonary disease. No cause is identified in 20% to 50% of cases. Hemoptysis must be differentiated from pseudohemoptysis, which is blood that originates from nasopharyngeal or gastrointestinal sources. The initial evaluation includes determining the severity of bleeding and stability of the patient and may require bronchoscopy for airway protection. Mild hemoptysis comprises more than 90% of cases and has a good prognosis, whereas massive hemoptysis has a high mortality rate. A history and physical examination can assist in identifying an etiology, but diagnostic testing is often required. Chest radiography is a good initial test, but it has limited sensitivity for determining the site and etiology of the bleeding. Computed tomography and computed tomography angiography of the chest with intravenous contrast are the preferred modalities to determine the etiology of bleeding; however, bronchoscopy may also be needed. In addition to supportive medical treatment, management should include treatment of the underlying etiology because recurrence often takes place in the absence of treatment of the identified cause. Bronchial arterial embolization is used to treat massive hemoptysis, particularly when an involved artery is noted on computed tomography angiography. Surgery is reserved for patients whose medical treatment and embolization are not effective.
Topics: Angiography; Bronchial Arteries; Bronchoscopy; Embolization, Therapeutic; Hemoptysis; Humans
PubMed: 35166503
DOI: No ID Found -
Autopsy & Case Reports 2022Endobronchial lipomas are rare benign lung tumors that can cause bronchial obstruction and parenchymal damage. While an uncommon etiology, they are often misdiagnosed...
Endobronchial lipomas are rare benign lung tumors that can cause bronchial obstruction and parenchymal damage. While an uncommon etiology, they are often misdiagnosed due to a clinical presentation similar to obstructive pulmonary pathologies such as COPD and asthma. Upon review of English-language literature, under 50 cases of endobronchial lipomas were documented in the prior 10 years (2011-2021). There are no clear guidelines regarding the management of this particular entity, but typically interventional debulking is the treatment of choice. Here we present another unique case of endobronchial lipoma along with our diagnostic and therapeutic methodology. The patient underwent bronchoscopic debulking via a cryotherapy probe. Based on the histopathologic analysis, a diagnosis of endobronchial lipoma was made. Endobronchial lipomas must remain in any clinician's differential when a patient presents with dyspnea. We report the unique location of this lipoma based on our literature review and the importance of investigating endobronchial lesions due to a possible diagnosis of endobronchial lipoma.
PubMed: 35574045
DOI: 10.4322/acr.2021.377 -
American Journal of Respiratory and... Sep 2020Chronic bronchitis (CB) is characterized by productive cough with excessive mucus production, resulting in quality-of-life impairment and increased exacerbation risk.... (Randomized Controlled Trial)
Randomized Controlled Trial
Chronic bronchitis (CB) is characterized by productive cough with excessive mucus production, resulting in quality-of-life impairment and increased exacerbation risk. Bronchial rheoplasty uses an endobronchial catheter to apply nonthermal pulsed electrical fields to the airways. Preclinical studies have demonstrated epithelial ablation followed by regeneration of normalized epithelium. To evaluate the feasibility, safety, and initial outcomes of bronchial rheoplasty in patients with CB. Pooled analysis of two separate studies enrolling 30 patients undergoing bilateral bronchial rheoplasty was conducted. Follow-up through 6 months (primary outcome) and 12 months included assessment of adverse events, airway histology, and changes in symptoms using the Chronic Obstructive Pulmonary Disease (COPD) Assessment Test and St. George's Respiratory Questionnaire (SGRQ). Bronchial rheoplasty was performed in all 30 patients (63% male; mean [SD] age, 67 [7.4]; mean [SD] postbronchodilator FEV, 65% [21%]; mean [SD] COPD Assessment Test score 25.6 [7.1]; mean [SD] SGRQ score, 59.6 [15.3]). There were no device-related and four procedure-related serious adverse events through 6 months, and there were none thereafter through 12 months. The most frequent nonserious, device- and/or procedure-related event through 6 months was mild hemoptysis in 47% (14 of 30) patients. Histologically, the mean goblet cell hyperplasia score was reduced by a statistically significant amount ( < 0.001). Significant changes from baseline to 6 months in COPD Assessment Test (mean, -7.9; median, -8.0; = 0.0002) and SGRQ (mean, -14.6; median, -7.2; = 0.0002) scores were observed, with similar observations through 12 months. This study provides the first clinical evidence of the feasibility, safety, and initial outcomes of bronchial rheoplasty in symptomatic patients with CB.Clinical trial registered with www.anzctr.org.au (ACTRN 12617000330347) and clinicaltrials.gov (NCT03107494).
Topics: Ablation Techniques; Aged; Bronchi; Bronchitis, Chronic; Disease Progression; Female; Follow-Up Studies; Forced Expiratory Volume; Humans; Male; Prospective Studies; Quality of Life; Time Factors; Treatment Outcome
PubMed: 32407638
DOI: 10.1164/rccm.201908-1546OC -
Frontiers in Immunology 2020Oxidative stress plays an important role in the pathogenesis of chronic obstructive pulmonary disease (COPD) caused by cigarette smoke and characterized by chronic... (Review)
Review
Oxidative stress plays an important role in the pathogenesis of chronic obstructive pulmonary disease (COPD) caused by cigarette smoke and characterized by chronic inflammation, alveolar destruction (emphysema) and bronchiolar obstruction. Ozone is a gaseous constituent of urban air pollution resulting from photochemical interaction of air pollutants such as nitrogen oxide and organic compounds. While acute exposure to ozone induces airway hyperreactivity and neutrophilic inflammation, chronic ozone exposure in mice causes activation of oxidative pathways resulting in cell death and a chronic bronchial inflammation with emphysema, mimicking cigarette smoke-induced COPD. Therefore, the chronic exposure to ozone has become a model for studying COPD. We review recent data on mechanisms of ozone induced lung disease focusing on pathways causing chronic respiratory epithelial cell injury, cell death, alveolar destruction, and tissue remodeling associated with the development of chronic inflammation and AHR. The initial oxidant insult may result from direct effects on the integrity of membranes and organelles of exposed epithelial cells in the airways causing a stress response with the release of mitochondrial reactive oxygen species (ROS), DNA, and proteases. Mitochondrial ROS and mitochondrial DNA activate NLRP3 inflammasome and the DNA sensors cGAS and STING accelerating cell death pathways including caspases with inflammation enhancing alveolar septa destruction, remodeling, and fibrosis. Inhibitors of mitochondrial ROS, NLRP3 inflammasome, DNA sensor, cell death pathways, and IL-1 represent novel therapeutic targets for chronic airways diseases underlined by oxidative stress.
Topics: Air Pollutants; Air Pollution; Airway Remodeling; Animals; Anti-Inflammatory Agents; Antioxidants; Cell Death; Environmental Exposure; Humans; Inflammation Mediators; Lung; Oxidative Stress; Ozone; Pneumonia; Pulmonary Disease, Chronic Obstructive; Pulmonary Emphysema; Reactive Oxygen Species; Signal Transduction
PubMed: 32983127
DOI: 10.3389/fimmu.2020.01957 -
BMJ Case Reports Feb 2022Rhinosporidiosis is a chronic mucocutaneous granulomatous disease caused by , commonly affecting the nose and nasopharynx. Endobronchial involvement is of rare...
Rhinosporidiosis is a chronic mucocutaneous granulomatous disease caused by , commonly affecting the nose and nasopharynx. Endobronchial involvement is of rare occurrence but can pose challenging problems for diagnosis, surgical excision and anaesthetic management. We report a 40-year-old man with a history of recurrent nasal rhinosporidiosis who presented with unilateral nasal obstruction, cough, shortness of breath and a radiological feature of left lung collapse. Eight years since the last surgery, he presented with a recurrent lesion in the nose with concurrent endobronchial involvement. The patient underwent excision of the nasal and the endobronchial lesion successfully under general anaesthesia without any complication and good symptomatic improvement. The clinical presentation and the management of endobronchial rhinosporidiosis are discussed here. The surgical difficulties faced during the procedure are highlighted.
Topics: Adult; Animals; Bronchi; Humans; Male; Nasal Obstruction; Nose; Rhinosporidiosis; Rhinosporidium
PubMed: 35140090
DOI: 10.1136/bcr-2021-247133 -
International Journal of Chronic... 2022Macrophage polarization plays an important role in the pathogenesis of COPD emphysema. Changes in macrophage polarization in COPD remain unclear, while polarization and...
BACKGROUND
Macrophage polarization plays an important role in the pathogenesis of COPD emphysema. Changes in macrophage polarization in COPD remain unclear, while polarization and ferroptosis are essential factors in its pathogenesis. Therefore, this study investigated the relationship between macrophage polarization and ferroptosis in COPD emphysema.
METHODS
We measured macrophage polarization and the levels of matrix metalloproteinases (MMPs) in the lung tissues of COPD patients and cigarette smoke (CS)-exposed mice. Flow cytometry was used to determine macrophage (THP-M cell) polarization changes. Ferroptosis was examined by FerroOrange, Perls' DAB, C11-BODIPY and 4-HNE staining. Nuclear receptor coactivator 4 (NCOA4) was measured in the lung tissues of COPD patients and CS-exposed mice by western blotting. A cell study was performed to confirm the regulatory effect of NCOA4 on macrophage polarization.
RESULTS
Increased M2 macrophages and MMP9 and MMP12 levels were observed in COPD patients, CS-exposed mice and THP-M cells cocultured with CS extract (CSE)-treated human bronchial epithelial (HBE) cells. Increased NCOA4 levels and ferroptosis were confirmed in COPD. Treatment with NCOA4 siRNA and the ferroptosis inhibitor ferrostatin-1 revealed an association between ferroptosis and M2 macrophages. These findings support a role for NCOA4, which induces an increase in M2 macrophages, in the pathogenesis of COPD emphysema.
CONCLUSION
In our study, CS led to the dominance of the M2 phenotype in COPD. We identified NCOA4 as a regulator of M2 macrophages and emphysema by mediating ferroptosis, which offers a new direction for research into COPD diagnostics and treatment.
Topics: Animals; Disease Models, Animal; Emphysema; Epithelial Cells; Ferroptosis; Humans; Macrophages; Mice; Nuclear Receptor Coactivators; Pulmonary Disease, Chronic Obstructive; Pulmonary Emphysema; Nicotiana
PubMed: 35386390
DOI: 10.2147/COPD.S354896